Arsenate and perchlorate toxicity, growth effects, and thyroid histopathology in hypothyroid zebrafish Danio rerio

Exposure to perchlorate or other thyrotoxic compounds can cause hypothyroidism in most vertebrates, and this may affect levels of endogenous antioxidants and cause oxidative stress. Arsenic also induces oxidative stress in animals by modifying the antioxidant capacity and may alter the thyroid homeostasis. Therefore, hypothyroidism may affect the toxicity of arsenate. In order to test this hypothesis, zebrafish (Danio rerio) were made hypothyroid by exposure to perchlorate, and toxicity of arsenate in hypothyroid and euthyroid fish was compared. The endpoints were LC50 and thyroid histopathology. Additionally, the recovery of thyroid histopathological indices after cessation of perchlorate exposure was determined. The current study showed that 96 h LC50 of perchlorate anion and arsenate ion to juveniles fish (37 day post-fertilization) were 2532 and 56 mg l−1, respectively. In addition, hypothyroid fish were more sensitive to arsenate, with a 96 h LC50 of 43 mg l−1. Growth rates were also significantly retarded by perchlorate exposure. After cessation of perchlorate exposure, there was recovery of thyroid histopathology in terms of epithelial cell height, but not colloid area or growth rate. In conclusion, perchlorate enhances arsenate toxicity to juvenile zebrafish, and the rate of thyroid recovery after cessation of perchlorate exposure depends on the endpoints examined.